Go to JCI Insight
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Publication alerts by email
  • Advertising
  • Job board
  • Contact
  • Clinical Research and Public Health
  • Current issue
  • Past issues
  • By specialty
    • COVID-19
    • Cardiology
    • Gastroenterology
    • Immunology
    • Metabolism
    • Nephrology
    • Neuroscience
    • Oncology
    • Pulmonology
    • Vascular biology
    • All ...
  • Videos
    • Conversations with Giants in Medicine
    • Video Abstracts
  • Reviews
    • View all reviews ...
    • Complement Biology and Therapeutics (May 2025)
    • Evolving insights into MASLD and MASH pathogenesis and treatment (Apr 2025)
    • Microbiome in Health and Disease (Feb 2025)
    • Substance Use Disorders (Oct 2024)
    • Clonal Hematopoiesis (Oct 2024)
    • Sex Differences in Medicine (Sep 2024)
    • Vascular Malformations (Apr 2024)
    • View all review series ...
  • Viewpoint
  • Collections
    • In-Press Preview
    • Clinical Research and Public Health
    • Research Letters
    • Letters to the Editor
    • Editorials
    • Commentaries
    • Editor's notes
    • Reviews
    • Viewpoints
    • 100th anniversary
    • Top read articles

  • Current issue
  • Past issues
  • Specialties
  • Reviews
  • Review series
  • Conversations with Giants in Medicine
  • Video Abstracts
  • In-Press Preview
  • Clinical Research and Public Health
  • Research Letters
  • Letters to the Editor
  • Editorials
  • Commentaries
  • Editor's notes
  • Reviews
  • Viewpoints
  • 100th anniversary
  • Top read articles
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Publication alerts by email
  • Advertising
  • Job board
  • Contact
Top
  • View PDF
  • Download citation information
  • Send a comment
  • Terms of use
  • Standard abbreviations
  • Need help? Email the journal
  • Top
  • Version history
  • Article usage
  • Citations to this article

Advertisement

CorrigendumAutoimmunity Free access | 10.1172/JCI19301C1

Abnormal germinal center reactions in systemic lupus erythematosus demonstrated by blockade of CD154-CD40 interactions

Amrie C. Grammer, Rebecca Slota, Randy Fischer, Hanan Gur, Hermann Girschick, Cheryl Yarboro, Gabor G. Illei, and Peter E. Lipsky

Find articles by Grammer, A. in: PubMed | Google Scholar

Find articles by Slota, R. in: PubMed | Google Scholar

Find articles by Fischer, R. in: PubMed | Google Scholar

Find articles by Gur, H. in: PubMed | Google Scholar

Find articles by Girschick, H. in: PubMed | Google Scholar

Find articles by Yarboro, C. in: PubMed | Google Scholar

Find articles by Illei, G. in: PubMed | Google Scholar

Find articles by Lipsky, P. in: PubMed | Google Scholar

Published March 1, 2007 - More info

Published in Volume 117, Issue 3 on March 1, 2007
J Clin Invest. 2007;117(3):835–835. https://doi.org/10.1172/JCI19301C1.
© 2007 The American Society for Clinical Investigation
Published March 1, 2007 - Version history
View PDF

Related article:

Abnormal germinal center reactions in systemic lupus erythematosus demonstrated by blockade of CD154-CD40 interactions
Amrie C. Grammer, … , Gabor G. Illei, Peter E. Lipsky
Amrie C. Grammer, … , Gabor G. Illei, Peter E. Lipsky
Article Autoimmunity

Abnormal germinal center reactions in systemic lupus erythematosus demonstrated by blockade of CD154-CD40 interactions

  • Text
  • PDF
Abstract

To determine the role of CD154-CD40 interactions in the B cell overactivity exhibited by patients with active systemic lupus erythematosus (SLE), CD19+ peripheral B cells were examined before and after treatment with humanized anti-CD154 mAb (BG9588, 5c8). Before treatment, SLE patients manifested activated B cells that expressed CD154, CD69, CD38, CD5, and CD27. Cells expressing CD38, CD5, or CD27 disappeared from the periphery during treatment with anti-CD154 mAb, and cells expressing CD69 and CD154 disappeared from the periphery during the post-treatment period. Before treatment, active-SLE patients had circulating CD38bright Ig-secreting cells that were not found in normal individuals. Disappearance of this plasma cell subset during treatment was associated with decreases in anti–double-stranded DNA (anti-dsDNA) Ab levels, proteinuria, and SLE disease activity index. Consistent with this finding, peripheral B cells cultured in vitro spontaneously proliferated and secreted Ig in a manner that was inhibited by anti-CD154 mAb. Finally, the CD38+/++IgD+, CD38+++, and CD38+IgD– B cell subsets present in the peripheral blood also disappeared following treatment with humanized anti-CD154. Together, these results indicate that patients with active lupus nephritis exhibit abnormalities in the peripheral B cell compartment that are consistent with intensive germinal center activity, are driven via CD154-CD40 interactions, and may reflect or contribute to the propensity of these patients to produce autoantibodies.

Authors

Amrie C. Grammer, Rebecca Slota, Randy Fischer, Hanan Gur, Hermann Girschick, Cheryl Yarboro, Gabor G. Illei, Peter E. Lipsky

×

Original citation: J. Clin. Invest.112:1506-1520 (2003). doi:10.1172/JCI200319301.

Citation for this corrigendum: J. Clin. Invest.117:835 (2007). doi:10.1172/JCI19301C1.

During the preparation of the manuscript, errors were introduced into Figure 3 that affected paragraph 6 in Results. The corrected paragraph and figure appear below.

The authors regret this error.

Expression of differentiation and activation antigens during and after treatment of active-SLE patients with humanized anti-CD154 mAb (BG9588, 5c8). CD38positive B cells in the circulation of the active-SLE patients disappeared from the peripheral blood during the treatment regimen with humanized anti-CD154 mAb (Figures 2b, 2c, and 3a). Specifically, before the treatment regimen, 63.8% ± 4.1% of the B cells were CD38positive. At 4–8 weeks after initiation of treatment, the percentage of CD38positive B cells in the circulation had dropped to 22.7% ± 15.0% (P = 0.024 compared with before treatment). Withdrawal of treatment led to a reappearance of CD38positive B cells in the circulation (79.3% ± 8.6%) at the earliest time point tested, 2 months after treatment, at a percentage that was not different from the pretreatment percentage (P > 0.05). Of note, this trend was significant for both the pre-switch IgD+ (P = 0.018) and the post-switch IgD– (P = 0.022) B cell subsets.

Version history
  • Version 1 (March 1, 2007): No description

Article tools

  • View PDF
  • Download citation information
  • Send a comment
  • Terms of use
  • Standard abbreviations
  • Need help? Email the journal

Metrics

  • Article usage
  • Citations to this article

Go to

  • Top
  • Version history
Advertisement
Advertisement

Copyright © 2025 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

Sign up for email alerts